Molecular characterization of Bovine herpesvirus type 1 Indonesian isolates | Saepulloh

A striking characteristic of H. PARTICIPANTS: Although most of the work was performed by scientists at UNL, Dept of VBMS we do have an active collaboration with Dr. haemolytica may not enhance secondary parainfluenza-3 virus infection. Fax: 61 7 3365 4980. T. CpHV-1 can be isolated from the nose and/or vagina of infected animals. This may not be the complete list of references from this article.

Thus, the parental strain BoHV-1 LA was used as control for all vaccination experiments. The intact zinc RING finger of bICP0 is also necessary for the trans-activation of heterologous promoters (18, 37). The latency and reactivation cycle have a significant impact on the epidemiology and control of BHV-1. Moreover, such negative results in goats inoculated with CpHV-1 suggest a difference in the antigenicity of gE between BoHV-1 and CpHV-1. The virus replicates in the upper respiratory tract epithelium and local lymph nodes, before it enters the bloodstream by attaching to leukocytes. Prostaglandin E2-induced inhibition of interleukin 2 production, J. In the present study, we used this in vitro system to examine a possible link between BoHV-4 persistent infection and potential pathogenicity.

Both groups developed cross-neutralising antibodies during this experiment suggesting partial clinical cross-protection afforded by the two infections. A Time course of altered phospho-JNK(Thr183/Tyr185) and phosphor-p38MAPK(Thr180/Tyr182) following BHV-1 infection. Infection of bovine cells (10) or calves (53) leads to rapid cell death and an increase in apoptosis. These data show that calves vaccinated with a modified-live IBR vaccine are protected from challenge with either the mutant or the conventional virus. During latency, apparently no viral antigens are synthesized but the genomes of the latent viruses are present in the nuclei of long living cells, such as, e.g., neurones of the ganglia corresponding to the sites of peripheral replication. Following primary infection of respiratory and ocular epithelia, both BHV-1 and BHV-5 establish latency in trigeminal ganglia (TG) (6, 26). Like IRF3, IRF7 undergoes virus-induced activation and phosphorylation at its C terminus (2, 22, 31).

Immunocytochemistry techniques were applied to both types of samples to locate EHV-1 antigen. MALDI-TOF/MS identification of differentially expressed proteins. To analyze the effect of the exchange of these homologous glycoproteins in PrV’s natural host, swine, 4-week-old piglets were intranasally infected with 106 PFU of either wild-type PrV strain Kaplan (PrV-Ka), PrV-9112C2, or PrV-9112C2R, in which the PrV gB gene was reinserted instead of the BHV-1 gB gene. LR gene products inhibit cell cycle progression (Y. BHV-1 can induce apoptosis in peripheral blood mononuclear cells (PBMC) (11, 16) and bovine B-lymphoma (BL-3) cells (10). Virus was isolated from, or found by immunocytochemistry in, the pharyngeal tonsil of all calves examined, except for two weanlings on days 1 and 8. PCR examination of tissues collected at day 35 pi detected latent viral DNA predominantly in lumbosacral spinal segments.

As expected, a late transcript encoding glycoprotein C was not detected in TG of latently infected calves. Interestingly, only activated JNK facilitated the viral multiplication identified through both chemical inhibitor and siRNA. The results demonstrated that (i) recombination is a frequent event in vivo since recombinants (gC+/gE+ and gC−/gE−) were detected in all coinoculated calves, (ii) relative proportions of progeny populations evolved during the excretion period toward a situation where two populations (gC+/gE+ and gC−/gE+) predominated without fully outcompeting the presence of the two other detected populations (gC+/gE− and gC−/gE−), and (iii) after reactivation from latency, no gC+/gE− and gC−/gE− progeny viruses were detected, although gC+/gE− mutants, when inoculated alone, were detected after reactivation treatment. Antibodies to HHV-6 and CMV were Measured in patients undergoing Documented serological responses to HHV-6. Using tagged BoHV-1 recombinant viruses, it was determined that the pUL51 protein completely co-localized with the cis-Golgi marker protein GM-130. Off-campus UNL users: To download campus access dissertations, please use the following link to log into our proxy server with your NU ID and password. 1A to C).

Hoornaert, F. We examined the induction and activity of BHV-1-specific cytolytic CD4+ T lymphocytes (CTL) by stimulating peripheral blood mononuclear cells (PBMC) of cattle immunized with attenuated live BHV-1. Lennert Steukers, DVM, is a PhD-student in the Department of Virology, Parasitology and Immunology; Annelies P. We describe two DPHS cases, the first to occur in Italy, with clinicopathological findings suggesting a potential pathogenetic role of bovine herpesvirus-4 (BoHV-4). When you are done browsing please remember to return to this page and log out. Our group has been involved in investigations of two members of the family Pasteurellaceae, Mannheimia haemolytica and Haemophilus somnus, which illustrate some of the complexities that must be confronted. The LR gene, but not LAT, inhibits caspase 3 cleavage during productive infection.

The identification of the isolate has been confirmed by IFA. The cow was 1 of 50 moved between 2 farms approximately 5 days before the onset of clinical disease. Abstract – Bovine herpesvirus 1 (BoHV-1), classified as an alphaherpesvirus, is a major pathogen of cattle.